NANDI (RIP brother) wrote a lot about it at CEM .... intersting stuff. But I do bascially I agree with rodge. Real life experience does not always correlate with the theory

http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1295815

[QUOTE]: Horm Res. 1992;38 Suppl 1:63-7. Related Articles, Links


Thyroid function during growth hormone therapy.

Jorgensen JO, Moller J, Skakkebaek NE, Weeke J, Christiansen JS.

Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, Denmark.

Administration of growth hormone (GH) in GH-deficient patients has been reported to cause a variety of perturbations in thyroid function. Reports range from decreased sensitivity of thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) stimulation and induction of hypothyroidism to increased energy expenditure and enhanced peripheral thyroxine (T4) to triiodothyronine (T3) conversion. Some of the diversities may relate to the fact that earlier studies were uncontrolled case reports, which furthermore employed pituitary GH preparations, which may have been contaminated with TSH. A confounding variable in terms of incipient TSH insufficiency in some patients may also have been present. Data from a placebo-controlled crossover study of 4-months GH therapy in GH-deficient adults, some of whom were on ongoing T4 substitution, revealed that the most prominent effect on thyroid function was increased peripheral T4 to T3 conversion without significantly affecting TSH levels or secretion from the thyroid gland. It was furthermore observed that T3 levels during placebo were significantly decreased compared to an untreated healthy control group. Comparable findings have been made in a controlled study of 6-months GH therapy in adult-onset GH-deficient patients. More recent data suggest that these effects prevail after long-term (16 months) therapy. Similar findings have also been reported in healthy subjects receiving pharmacological GH doses. It is likely that this effect is not caused by GH per se inasmuch as reduced T4 to T3 conversion is a common observation in catabolic states with concomitant GH hypersecretion. It remains to be shown whether insulin-like growth factor I (IGF-I) stimulates peripheral deiodination.
http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1619991


Effects of growth hormone administration on fuel oxidation and thyroid function in normal man.

Moller J, Jorgensen JO, Moller N, Christiansen JS, Weeke J.

University Department of Internal Medicine and Endocrinology, Aarhus Kommunehospital, Denmark.

In a randomized, double-blind, placebo-controlled, cross-over study, we examined the effects of 14 days of growth hormone (GH) administration (12 IU/d subcutaneously) on energy expenditure (EE), respiratory exchange ratio (RER), and thyroid function in 14 normal adults of normal weight (eight men and six women). EE (kcal/24 h) was significantly elevated after GH administration (2,073 +/- 392, [GH], 1,900 +/- 310, [placebo], P = .01). RER was significantly lowered during GH administration (0.73 +/- 0.04 v 0.78 +/- 0.06, P = .02), reflecting increased oxidation of lipids. Total triiodothyronine (TT3) (nmol/L) and free T3 (FT3) (pmol/L) increased significantly during GH (TT3: 1.73 +/- 0.06 [GH], 1.48 +/- 0.08 [placebo], P = .01; FT3: 6.19 +/- 0.56 [GH], 5.49 +/- 0.56 [placebo], P = .01). Concomitantly, an insignificant decrease in reverse T3 (rT3) (nmol/L) was observed (0.07 +/- 0.01 [GH], 0.15 +/- 0.01 [placebo], P = .08). GH caused a highly significant increase in T3/thyroxine (T4) (x 100) ratio (1.84 +/- 0.12 [GH], 1.37 +/- 0.06 [placebo]). Serum thyrotropin (TSH) was not significantly changed by GH. No changes in total thyroxine (TT4) (nmol/L) (98 +/- 6 [GH], 111 +/- 8 [placebo], P = .40) and free thyroxine (FT4) (pmol/L) (17.4 +/- 1.3 [GH], 18.6 +/- 1.1 [placebo], P = .37) after 14 days of GH administration were observed. In conclusion, 2 weeks of GH administration increases EE and lipidoxidation. This finding may partly be mediated by an increase in peripheral T4 to T3 conversion